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Glucocorticoid-Induced Osteoporosis Responds to Denosumab

Glucocorticoid-Induced Osteoporosis Responds to Denosumab

At 12 months, denosumab significantly increased spine and hip bone mineral density as compared with risedronate, suggesting denosumab may be a treatment option for glucocorticoid-induced osteoporosis.

This is according to research by Kenneth S. Saag, M.D., of University of Alabama at Birmingham, and colleagues, presented at the American College of Rheumatology annual meeting held in Washington, D.C. on Nov. 15.

Glucocorticoid (GC)-induced osteoporosis (GIOP) is the most common secondary cause of osteoporosis. The American College of Rheumatology plans to issue updated recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis in 2017. ACR last updated its GIOP recommendations in 2010.

Glucocorticoid-induced osteoporosis (GIOP) is associated with decreased osteoprotegerin expression and it is characterized by an increased osteoprotegerin receptor of the RANKL pathway —or, receptor activator of nuclear factor kappa-B ligand (RANKL). Denosuma­­­b is a monoclonal antibody to RANKL.

Researchers compared the safety and efficacy of denosumab with risedronate in a phase 3 double-blind, active-controlled study of 795 glucocorticoid-continuing and glucocorticoid-initiating subjects over 24 months. This is 12-month data from that study of adult patients who had a history of osteoporotic fracture. Glucocorticoid-continuing participants (representing 505 subjects) who were at minimum, 50 years old, had a history of lumbar spine, total hip or femoral neck bone mineral density T-score of less than or equal to -2.0 or a T-score of -1.0 or less with a fracture history.

Subjects were randomized to a 60 mg subcutaneous dose of denosumab every six months or oral risedronate 5 mg daily for 24 months. Participants also received 1,000 mg or more of daily calcium and 800 IU or more vitamin D supplementation.

The international group of researchers found that, at 12 months, denosumab treatment was superior to risedronate among glucocorticoid-continuing and glucocorticoid-initiating subgroups, demonstrating greater gains in bone mineral density in the lumbar spine and total hip. The change in lumbar spine bone mineral density from baseline to one year in the glucocorticoid-continuing was 2.3 percent among those taking risedronate versus 4.4 percent in the denosumab arm. The percent change in total hip bone mineral density in the glucocorticoid-continuing group was 0.6 percent in the risedronate group versus 2.1 percent in the denosumab group at one year. Bone mineral density in the lumbar spine changed 0.8 percent among those taking risedronate in the glucocorticoid-initiating group versus a 3.8 percent change in the denosumab arm, and the change in total hip bone mineral density was 0.2 in the risedronate compared to 1.7 percent in the denosumab group.

Adverse events, including severe events, such as infection and fracture, occurred at similar rates between the denosumab and risedronate treatment arms.

There are approved therapies for prevention or treatment of glucocorticoid-induced osteoporosis; yet, many candidates for treatment do not receive it. Denosumab has the potential to become a treatment option for patients just starting or continuing glucocorticoid treatment, who are at fracture risk, write the authors.

The study is ongoing.

 

Disclosures

Dr. Saag and the study co-authors have ties with or are employed by Amgen, the maker of Prolia (denosumab injection).

 

References

 
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